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5-1-1935

Etiology of angina pectoris with special reference to coronary

spasm
John A. Kahl
University of Nebraska Medical Center

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Kahl, John A., "Etiology of angina pectoris with special reference to coronary spasm" (1935). MD Theses.
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 ~TICLOGY CF A.NGINA PECTORIS
UTH SFSCIAI HEFEHENCE TC C()RCNARY SPASM ~lS TH'G CAll ::'E.

BY
John A. Kahl.
 Dedlcated
to the memory of
iliIT FATHER.
I present this thesis to the facuJity of
The University of Nebraska, School of Med-
icine, as partial fulfill~ent of my vork
for the degree of Doctor of Medicine.
1935.

480706
 INTRODUCTION.

The etiology of angina pectoris has been at d~agreemant

since the first recogni. . t~on of the disease.

Theories have been advanced by the hundreds, the vie'ilTs as
to th,,:, one must sound havecredominated the medical field
at different areas.
The .3ul}ject originally chcosen W3.S Coronary Spasm,
but it b":'came arp;~rent that the other theories and ideas
'.<11ould have to be considered.
The old literature 'Vas of little value, excel·t as a histor-
ic:al purpose, and the undsr-standing of the old theories.
The most of this '."lork had to be t:aken from recsnt<fwrk,
mostly fron; journals and papers.
To narrow' the field to corornary spasmt\~the cause,
''ilhile believed by most of the leading authori ties, has
only recently found suffieient evidence to roake it mor,,:,
than a theory. But one cannot forget that there are
still cases for argument.

I have tried to cover the literB.ture for lastfive years,

a ttempting to present all the argument5! and expirmenta.l
ev!ildence found,) in a clear manner. But the question is
f3.r from finished and it will :~take considerable work
to put thJ3 IJI'esent ideas on a sound footing.
 Angina pectoris the "Meditates monte" of Seneca of anc-
ient literature Was first described only 164 years ago by
Heberden, is by no means a disease of recent origin.
Hippocrates undoubtedly observed some cases, although
he did not mention any symptoms, there are never 0he less re-
ferences in ancient literature which undoubtedly were ang-
ina, the most famous of these writings, is the description
by Seneca, villo told of the suddenness of the onset of an at-
( 1)
tack with the impetuousity of a te~pest.

Dionis, surgeon to Louis XIV, described two cases which

were either Angina or its closely allied syndrome, coronary
occulsion.
Hoffman in 1734 and Mergayni in 1689 described cases
'liThi ch were undoubtedly angina pectoris, the most famous be-
ing that report of Morgayni, of a well known Italian physic-
ian Ferrianni who died of this c')ndi tion, on who a post-mor-
( 1)
tern was done. In France Roughnon, in February 1768,
just five months previous to Heberden's description, des-
cribed in a letter to Lorry, a case of a cavalry officer
::Ionsieur Charles Captain of the Cavalry, wh.ich was the near-
est complete description previous to Heberden. Most French
authors claim this as the first description of angina pect-
oris. Huchard quoting Rougnonts letter, does not use any ex-
pression which descrt bed pain as a sympti)m in the attacks,
but Osler, on the other hand, who had evidently seen a copy
of the original letter, quotes sever~l sentences showing that
 the feeling of suffocation felt by the patient was associat~

ed with pain of great intensity and believes that the sudden-

ness of the attack, the pain in the region of the heart, the
abrupt termination, and mode of death following exertion
after a full meal, favors the decision of a true angina pe-
( 2)
ctoris.
Gaidiner quotes the philosopher Seneca as evid.ently
suffering from the dlhsease, although there is e. dispute as
( 2)
to the meaning of Seneca's words.
But there is no doubt that Heberden was the first to
~ot
give a complete description of angina, but he did separate
pain from anguish and fear of death. But never-the-less it
was a master piece. As HarloW Brooks states, "There are few
instances in medical literature Which equal in clarity, in
detail of keen observation and in practical accuracy of ap-
plication, the original publication of Heberden's. Heber-
den's article to-day stands as the most satisfactory and gr-
aphic description of the clinical picture which has yet been
written. There is little to be found in any modern article,
except as dealing with the etiology pathology, physiology
and treatment of the subject which is so complete and accur-
(3)
ate as this study.
In 1768, in Transactions of the London College of Phy-
sicians, Heberden wrote an article entitled IIS ome Account of
a Disorder of the Breast.'f The article Was not long but
,_ very complete, and is as follows.
t~There is a disorder of the breast, marked Iith strong and
peculiar symptoms, considerable for the kind of danger be-
longing to it, and not extremely rare, of which I do not
recollect any mention among medical authors~ The seat of
it, and the sense of st ..r"angling and anxiety with which it
is attended, may make it not improperly be called Angina
pectoris.
Those, who are afflicted with it, are seized, while
walking, and more particularly when they walk soon after eat-
ing, with a painful and most disagreeable sensation in the
breast, which seems as if it would take away their life, if
it were to increase or to continue; the moment they stand
still, all uneasiness vanishes. In all other respects, the
patients are, at the beginning of this disorder, perfectly
well, and in particular have no shortness of breath, from
which it is totally different.
After it has c:)ntinued some months , it will not cease
so instantaneously upon standing still; and will come on,
not only when the persons are walking, but when they are ly-
ing down, and oblige them to rise up out of their beds every
night for many months together; and in one or two very invet-
erate cases it has been brought on by the motion of a horse,
or a carriage, and even by swallowing, coughing, going to
stool or speaking, or by any disturbance of the mind. I
have heard, one, and only one person say that he had known
,tt att,ack him, while he was up and standing still or sitting.
 But most, whom I have seen, have been perfectly unaffected
with riding in any manner, with speaking, swallowing, laugh,.
ing, sneezing, or vomiting. One has told me, that this com-
plaint was greatest in Winter; another, that it was aggrav-
ated by Warm weather; in the rest, the seasons were not sus-
pected of making any difference .
.
I have observed something like this affection of the
breast in one woman who was paralytic, and have heard one or
two young men cooplain of it in a slight degree; but all the
rest, whom I have seen, who are at least twenty, were men,
and almost all above fifty years old, and most of them with
a short neck, and inclining to be fat.
When a fit of this sort comes on by walking, it's durat-
ion is very ShOI~, as it goes off almost immediately upon
stopping. If it comes on in the night, it will last an hour
or two; and I have met with one, in whom it once continued
several days, during all Which time the patient seemed to be
in imminent danger of death.
When I first took notice of this distemper, and could
find no satisfaction from books, I consulted an able physic-
ian of long experience, who t)ld me that he had known several
ill of it, and that all of them had died suddenly. This ob-
servation I have reason to think is generally true of such
patients, having known six of those, for whom I had been con-
sul ted, die in this manner; and more perhaps may hGtve exper-
,K_ ienced the same death, which I had no opportunity of knowing.
But though the natural tendency of this ill:!b.ess be to kill
the patients suddenly, ~et unless it have a power of preserv-
ing a person from all other ails, it will easily be believed,
that some of those who are afflicted with it, may die in a
different manner, since this disorder will last, as I have
known it more than once, near twenty years, and most usually
attacks only those who are above fifty years of age. I have
accordingly observed one, who sunk under a lingering illness
of a different nature.
The os sterni is usually pOinted to as the seat of this
malady, but it seems sometimes as if it were under the lower
part of it , and at other times under the middle or upper
I

part of it, but always inclining more to the left Side, and
someti'~)es there joined with pain about the middle of the left
arm. Yfuat the ps,rticular mischief is, which is referred to
these different parts of the sternum, it is not easy to guess,
I have had no opportunity of knowing with certainty. If may
be a strong cramp, or an ulcer, or possibly both.
The opinion of it being a convulsion of the part affect-
ed will reao_ily present i teelf to anyone, who conSiders the
sudden manner of' it coming on and going off; the long inter-
vals of perfect ease; the rf:;lief af .horded by wine and spiri t-
uous cordials; the influence, which pa,ssionate affections of
the mind have over it; the ease which comes rrom varying the
posture of the head and shoulders, by straitening the verte-
brae of the thorax or by bending them a little forward or back-
wards; the number years, Which it will continue with out oth-
er wise disordering the health; its generally bearing so
well the motion of a horse, or carriage, which circumstances
after di stingui she s spasmadi c pains ::'rom those which ari se
tram ulcers; and lastly, its c;)ming on in certain patients at
night, just after th.e first sleep, at which time the incubus,
convulsive, asthmas, numbness, epilepsies, hyponcondriac
languol.'s, 8.nd other illS justly attributed to the di sturbed
functions of the nerves, are peculiarly apt either to return
or to be aggravated •
The pulse is, s.t least sometime s, not disturbed by this
pain, and consequently the heart is not affected by it; which
I have had an oP90rtunity of knowing by feeling the pulse dur-
ing the paroxysm; but I have never had it in my power to see
anyone ,opened, who had died of it; the sudden death of the
patients adding so much to the common difficulties of making
such an enquiry, that most of those, with whose cases I have
seen acquainted, were buried before I had heard that they were
dead.
But though it be most probable that a strong spasm be
the true cause of this disease yet there is some reason for
thinking, that it is sometimes accompanied with an ulcer, and
may partly proceed from it; for I have seen two of these pat-
ients who aften use to spit blood and purulent matter, one
of whom constantly asserted that he felt it come from the
sBat of the disorder. Another had a painful sensation in
 swallowing, and upon pressing the part, Which seemed to be af-
fected. From a. fourth, who fell down dead without any notice
there i~mediately arose such an offensive smell, as made all
who happened to be present, judge, that some foul abcess had
just then broken.
Bleeding, vomits and other enoculatlons, have not appear-
ed to me to do any good. Wine and cordials taken at going to
bed will prevent, or weaken, the night fits; but nothing does
this so effectually as opiates. Ten, fifteen or twenty drops
of Tinctura Theloina taken at lying down will enable those to
keep their bed until morning, who had been I'oroed to rise, and
sit up two or three hours every night, for man~ months. Such
a quantity OE a greater might safely be continued, as long as
it is required; and this relief afforded by opium maybe add-
ed to the arguments, which prove these fits to be of a oon-
vulsive nature. Time and attention will undoubtedly dis-
cover more helps against this trying and dangerous ailment;
but it is not to be expected, that much can have been done
towards establishing the method of cure for a distemper 11.i-
therto so umloticed, that it has not yet, as far as I know,
(4~
found a place or a name in the history of diseases."
Jenner was the first to describe the association of the
( 2)
disease of the coronary arteries with angina. This was
done in a letter to Heberden in 1776 after J entler had seen
the famous John Hunter, who had his first attack of angina
~. pectoriS in 1773 and his second 1776. Jenner did not pub-
 lish his letter, as he did notc<ish that Hunter should know
and see his opinion. Hunter suffered for twenty years from
angina pectoris, and, as it is known, died at a meeting of the
Hospital Board of the St. John's Hospital in October 1793.
Further descriptions of the disease were published by Froth-
ergill, Parny, P.M. Lanthom, Stokes and other English physic-
ians. Allan Burns, in 1809 was the first to bring forth the
( 2)
theory of intermittant claudications.
Huchard collected 64 different opinions from many well-
known physicians as to the cause of angina pectoriS, a few
of these will be mentioned. Rougnon and Heberden, as shown,
believed in a spasm of the heart, Hunter and Jenner believed
it to be due to ossification of the coronary arteries. Parry
considered as possible a spasmodic condition of the myocar-
dium, a momentary exaggeration of an existing feebleness of
the heart. Frothergill, because most of the patients were 0-

bese, thought it was the result of fat in the mediastinman.

P.M. Lanthom Was the first to consider angina as a symptom
( 2)
complex and not a disease.
Virchow, Cbhnheim and Qerain believed it to be due to
embolism, or thrombosis of' the coronary arteries. Bouil-
land and Bucqury believed that there were two types of angina
( 2)
pectoriS, one coronary and the othei neuralgic or neuritis.
Trousseau was of the belief that angina pectoriS was a form
of epilepsy. Sir James Mackenzie in his latest writing be-
".-. ... lieves it due to an exhaustion of the cardiac muscle and in
other places he speaks of it as if it w'ere of nervous or va-
Bcular origin. Verdon believes it is a neurosis of the var-
ious segments of the cord, in which the neurons show evidence
of infla"'lmatory proces se s.
The last importants discovered vvasthat of Louder Brun-
ton who was the first to suggest the use of nitrites in the
( 1)
vascular spasm.
So in suming up this brief history, the outstanding
contributions concerning angina pectoriS Was first Heberden
who gave the first complete clinical dese~tption of the dis-
ease, second Jenner was the first to associate the clinical
syndrome with diseases of the coronary arteries and third and
last Louder Brunton who was the first to give a treatment
which would relieve the attacks, the use of nitrites, now let
us turn to a brief resume of the anatomy and physiology of
the blood sU901y to the heart.
 If)

The blood supply to heart is mainly through two coronar-

iesarteries. The left divides almost immediately after lea-
ving the aorts, into the left circumflex and a larger ant
~mus descendens. The former runs in the atrio-ventricular
groove to the left terminating in a descending poster~OD ra-
mus. The anterior descending ramus encircles the pulmon-
ory artery on its left and runs downward in the interven-
tricular septum to the apex. Near its orgin sept.n branch-
es are given off. The right coronary artery runs to the
right in the fat of the atrio-ventricular sulcus and term-
inates posteriorly in several descending branches in the
right ventricle. Special twigs supply the Sino-aricular node
and conducting system. Considerable variation occurs in the
disti"ibution and anastO'TIoses of the several branches, both
in different species and in different hearts of the same
species. It is also probable that considerable modification
in vasculorization of different areas occurs as age advances,
this being certainly true as a sequence of disease. Gross
believes that the left coronary develops more extensilZe an-
astomosis and its branches supply increasingly greater areas,
with greater numbers of tributaries as the individual be-
comes older. This left coronary preponderance is probably a
morphageral compensation for the gradually developing fibra.-
tic changes.
The branches of the main coronary ~ami pass superfically
!"""". in the general dire cti on of the apex, and from the se intra-
mural branches run directly inward - more perpendicularly in-
to the left than into the right ventricular muscle. These
subdivide repeatedly and form very extensive capillary plex-
uses around the muscle elements. The endothelial cells of
these capillaries appear to form the boundaries of the lymph
channels.
According to most authorities inter arterial anastom-
oses between branches of the same and (ifferent rami are nu-
merous particularly in the enterventricular septum, roots of
( 1)
the large vessels and in the auricles.
In addition there are three subsitiary systems of arter-
i al anastomose s exi st; first an:::extensi ve anastomosi s between
the coronary branches and extra cardiac branches of the 13,-

orta, particularly at the site of the pericardial reflection

around the oste ... of large veins, second.arterio-luminal
ves~els running directly from the cononary arteries into the
cavities of the heart and last the arterio-siuasoidol vessels
communicating wi th ventricular cB.vi ties by means of myocard-
( 1)
i al sinusoids.
The coronary arteries belong to the muscuLi!' tyoe of
artery with three coats, the intima, media and adeuentia. Be-
fore Edholm (1912) reported his studies, little or nothing
was written as to the normal histology of the coronary art-
eries, little Was done until 1923, Wolkoff published his st-
( 2)
udy of nine hearts of different ages. McLeans work on
95 hearts supported the following 1) The small muscular art-
eries of the myocardium and the small epicardial arteries have
a similar picture in normal healthy individuals, that is an
intima bounded internally by a single layer of endothelial
cells and externally by a vaxy internal elastic lamina be-
tween which there is only a small amount of fine fibrous ti-
ssue. In the intima of the smallest arteries there is no fi-
brous tissue. The internal elastic lamina as McMeans has
pOinted out, consists of an acellular band of homogenous mat-
erial, which under certain conditions will split and disclose
its inner composition. This seems to be a laminated structure
of fine fibrillar material. McMeans has shown that any infl-
ammatory or toxic SUb~ctinf is sufficient conscentrations
results in a dissolution or alteration in the sheath of this
elastic lamina and gives the appearance of splitting, once
induced is permanent and maybe increased by further injury_
The media is made up of involuntary smooth muscle fibers, var-
ies in thickness with the diameter of the lumen. Between
the muscle fibers which run in a circular direction, is the
small amount of fine fibrous tissue Showing a small number
of fine elastic fibrils. The external coat on adventia con-
sists of loose connective tissue bundles made up of collagen
fibers inter-mixed with a considerable number of elastic fi-
brills and some muscle cells. As a rule this coat in the
smaller arteries is two or three times the thickness of the
media. The elastic tissue rarely forms 8, trtue external el-
nstic lamina. In the medium sized arteries (a group usually
 la

made of the descending and circumflex branches of the coron-

ary arteries which run in the epicardial fat) the intima pre-
sents a few longitudinal muscle fibers lying internal to the
( 2)
internal elastic layer.
The right and left Coronaries, the larger arteries, who-
se coats follow roughly the same proportional sizes to one
anbther as those in the medium sized arteries. Small nutr-
ient vessels and sympathetic nerve fibers are found through-
out the adventia of these main stems. It has not been pos-
sible to determine definitely how far inward these nutrient
vessels pass in a normal coronary, but in sclerosis they have
( 2)
seen to pass the entire wall into the inti~a.

Physiologists have long known the heart has a double ner-

ve controll, the cardio-inhibitory nerves (vagus) and cardio-
occelarator the sympathetics. It is also known that these
nerve fibers accompany the blood vessels,the coronaries as
(3) PP 254
wel~as shown by degeneration experiments.
Experiments of sutton and Lueth appeared to de~onstrate

conclusively that sudden mechanicsl constriction of the cor-

onary vessels invariably gives rise to pain, referred to the
left foreleg of dogs. The nerve fibers concerned accompany
the blood vussels and proceed over the sympathetic system,
for it was unaffected by vagus section and was aboliShed by
PQlnting the arterial walls with alcohol and by removal of
the stellate ganglion. The exact action of the two nerves
syste:ns is, still questionable, but it is thought that the va-
gus is the pressor to the coronary arteries. It was found
that section of the vagus caused an increased coronary flow,
but stimulation of the distal end caused a decreased coronary
flow and stimulation of the sympathetics causes an increase
(3 )
in blood flow through the coronaries.
 We shall now turn to the main theme of this subject.
Angina pectoris is a condition improperly named in order to
gi ve us any concept of it. It is a disease only recently
known to medicine as an entity in irif.Self, and there is still
some discussion as to whether it is suchJand not a complex
of symptoms.
This disease is not one of child-hood nor it is not un-
known in the aged and decayed. But its greatest prevalence
is at middle life, as autopsy study of 141 fatal cases of
angina showed, the average age of onset for men was 56 years
( 14)
and women 58.1 years. But angina in its typical mani-
festibns is far from unknown in young persons. Heberden re-
fers to case in a boy at 12 years, probably on a rheumatic
basis. Fothergill publishes two typical cases at 25 and 30
years. Allan Burn' 8 patient suff'ered it at ages 34 to 40
years, all of these probably being on syphilitic basis.
Vardon has seen two defini te cases in children 8,nd three
in adolescence, all of which ended in recovery, so they were
undoubtedly on a rheumatic basis. Dr. Hugh Stewart has pub-
lished a case in a boy age 7 years which come on at the con-
clUSion of a severe rheumatic fever, first indefinitely, and
then in frequent typical attacks, sudden pallor, pain and an-
xiety. Such was the child age l2t years Verdon saW in his
private practice. In these cases in young persons with heart
sounds, generally end in recovery, so far as the angina is
concerned. Many syphilitics develop angina between 40-50
 I'

and not rarely 25-35 years.

It is generally believed that this disease is one which
falls upon the upper classes, but AlJLbutt has not found it
quite so rare in hospitals as generally supposed. Both gout
and angina pectoris are supposed to be diseases of the easy
and intellectual classes, and both are not infrequently as-
sociated with high blood pressure, with the people as a whole
leading a sedentary life, consuming large quantities of rich
foods. ~utSomberger quotes seventy three cases in the Poly-
( 35)
clinic of Prague in 1895 to 1898, of poor working people.
In regard to sex, it is much more common in the males.
Husband two hundred and seventy three cases show the propor-
tion of one female in every sixty cases, Allbutt's show
( 35)
three in 100, and Osler 1 in every 40 cases. For this
great difference in sexual susceptibility no very definite ex-
planation C8,n be made, for the ~:matomy of the coronary art-
eries and the heart are the same. It has been said that the
difference may lie in some measure to a lower incidence of
syphilis and gout. Perhaps to some extent in a greater pro-
tection of the thoracic aorta from physical strain •.: -oThis
seems to point out that angina is not in the nature of a neu-
( 35)
rosis, otherwise it would be more prevalent in the female sex.
Heridity is considered to play no part in angina pector-
is, but nevertheless a proclivity seems to run in families
not infrequently. Robert Hamilton was the first to call at-
tention to this. Neuburger found 20 cases his 143 cases with
a blood kindred.
It is often stated that it is usual in angina pectoris,
to find a hereditary tendency to irritability of the nervous
( 35)
system, but Allbutt thinks it is not so.
Season change seems to have little influence on the in-
cidence of the disease, as was stated by Heberden, and agreed
to by subsequent teachers.
Allbutt seems to think that the causes of angina, have
much in common with the causes of any arterial disease. Fore-
most is phySici2,lJ,labor as upheld by Gibson, but this state-
ment should be qualified, because of the higher incidence of
shyphlis and rheumatism in the cities. When the first attack
does come on during exertion, it is usually of a mild type as
walking against a Wind, weilding of a fishing rod or a golf
club. The moments of most seizures are often determined by
effort, even by effort of mind or emotion. Yet Heberdon has
told us 8,ttacks come on during rest and even sleep. Didenot
died of angina, a very severe attack a'Noke him from sleep,
and so with many other cases.
Such nocturnal accesses ma~be in obedience to secret ti-
des of' blood pressure, as we must remember, apoplexy not in-
frequently occurs during sleep.
Tobacco seizures, whether a~ginal or cardiac orgin, oc-
cur at ghostly hours. It has been recently noted that smok@
i of cigarettes produces a marked temperature drop of sur-
face of fingers and toes, even tn the habitual user, the ave-
 o F.
age drop from one cigarette was 5.3 while the maxium was
of.
It was also found that this effect Was the result~,
of tobacco and not nicotine alone, as denicotinized cigarettes
had the same effect. The underlying cause was the vaso con-
.
striction as in the capillaries of natl bed, by slowing and
stoppage of blood.
So it is logical to think it might bring on the anginal
( 25)
attacks, by similar affects on the coronary arteries.
The strain of c',)ntinuous H.B.P. in order to d.amage the
arterial walls, must ha.ve run for years at excessive heights.,
It is the general idea, that angina pectoris is commonly seen
with a high blood pressure, but such is not the case as shown
by Epplinger and Levine. They found in 141 fatal cases of an-
gina that those he.ving normal blood pressure showed the dis-
ease begins about tour years earlier and lasts a little long-
er, but the age of death is an a.verage of three years sooner.
The blood pressure findings of the males of which there were
111 was an average of 149.2 systolic and 89.2 diastolic.
While corresponding figures for women were 190 systolic and
102 diastolic. It is also important to note that there were
46 men wi th a systolic reading under' 140 mm, there were no ;;
( 14)
women wi th such a L)W reading. It must also be remember-
ad that angina for the greater part, is a disease of the eld-
erly in whom pressures are notably a Ii ttle higher. Kauff- .
mann says that pain, with a normal heart, raises the minute
VOlume, the B.P. 8,nd the heart's work. So it may be that the
 '1

arterial pressure maybe driven up during an attack. This

seems to have been verified by Allbutt, Morrison, Mackenzie
( 35)
and Price. But Huchard and Porter say that pain causes
the B.P. to fall. But with all taken into consideration, we
might consider B.P. as having little rela~ion8hip to angina
pectoris. Allbutt is of the opinion that too much mental and
emotional strain is a basic cause for angina.
White lays emphasis on the stress and sp{3ed of modern,
life, and the news paper r'eports of frequent sudden deaths
seem to corroborate this contention. It has more or less been
accepted that brain workers at high tension are particularly
liable, but Ba8s end Donnor report that the incidence in the
working class is also high. Herrick is of the opinion that
this condition, like cancer, the apparent increase is partly
due to the fact tha,t larger numbers are reaching the senesc-
ent years.
~oW' we must get to the causes of this condition, trying
to find a reasonable and scientific basis. Since in coronary
thrombosis we find a Similar se~ of symptoms, and also elect-
ro-cardiogram Ch8Jlges. But in angina the pain is only tran-
sient as comp&.red to the coronary thrombosis.
With these facts we can begin to study the autopsy find-
ings in hope of finding an explanation of the disease. At
the present time we must consi<iier for pathology in angina
pectoris, three parts of the vascular system. first the lnvu-
Ivement of the coronary arteries, second the changes of the
first portion of the ascending aorta and, third the changes
in the cardiac musculature.
The defenders of the first hypothesis attribute pain to
ischemia caused by organic changes or spas~s of the coronary
vessels, many authors are inclined to believe that spasms are
usually ce,used by anatomic changes. Recent investigations
have shown that the heart as well as the coronary vessels
( 4)
possess sensory nerves and may perceive pain , this being
the basis for considering organic changes.
Koch and Kong made a special study of. serial sections
of hearts with special attention to the analysis of the
coronary circulation in cases of stenso~~s and occlusion of
the coronary artery. The Spalteholz's method of colored
injections and preparation of transparent specimens were
(12)
employed - • 'fhe specimens were obtained chiefly from
persons with typical angina pectoris. The only pathologico-
anatomic changes of the coronary arteries study were those
of artherosc1erotic and syphilitic processes, because they
dominated the circulatory disturbance. The three processes
responsible for occlUSion or stenosis of the coronary arter-
ies, were first, aDheroma, second, fibrous occlUSion and,
(~
third, thrombosis--very rarely endarteritis obliterans •
Frequently a combination of the three prossesses may be
found. Predominance of one of the forms allows a conclu-
sion as to the time of appearance. The non-caleifying
soft atheromatosis is of great importance for coronary
 occlusion while the calcifying arteries is of lesser import-
ance for circulatory disturbances in the cardiac muscle. Re-
coralization of occluSions generally can not be identified
with a communication of the interrupted section of blood
vessels; it takes place only in spaces extending to a later-
al br~nch; new lumina of vessels are formed also by the or-
ganization tissue in niches of altheromas. The syphilitic
coronary occluSion is the result of a lesion of the wall of
the aorta and not of the coronary arteries; usually the oc-
clusion is only a few millimeters thick and develops in the
course of a case of syphilis with a rapid course. When the
coronary circulation is affected by an occlusion as discuss-
ed, the rich formation of anastomoses of the cardiac circulat-
ion must be considered. Main anastomoses are l':)cated between
the areas of the right coronary and the circumflex arteries.
The diameters and ramifications of such branches vary consid-
erably. The anterior descending artery is an independent br-
anch with few anastomoses except in the lower portion leading
to the right coronary artery; therefore the above mentioned
artery is inclined to formation of infarcts Which, if confin-
ed to this area, are of minor functional importance. Occlus-
ions in the three-main coronary branches develop as follows:
in the proximal portion of the descending and in the periph-
eral portion of the other two branches. On account of the
formation of the lateral branches, the location of the occlus-
~"1;ons is of great significance. Cardiac infarcts may be ex-
 pected in angina pectoris, Which produces grave attacks or
death. In such cases usually an occlusion of two of the main
branches is found. A grave stensois in a blood vessel and
under development of one of the larger may create conditions
similar to an occlusion, but if an occlusion follows in the
second main branch, the picture resembles rather an acute car-
diac failure, than an attack of angina pectoris.- A Syphilit-
ic coronary occlusion is located close to the origin of .the
coronary arteries; therefore, the lateral branches can not
participate in collateral circulation; the occlusion develops
slowly, hence infarcts are relatively rare and formation of
anastomoses is prevented; sudden death and also attacks of an-
gina pectoris in cases with a sy':)hilitic coronary occlusion
are due to increasing limitation of the blood supply by a sin-
gle artery; sudden overloading caused by various factors pro-
duces ischemia of the entire heart with resulting insufficie-
ncy.
The soft antheroma is much more dangerous than one with
marked fibrous nodular development, because it rapidly fills
out the lumen and maybe accompanied by acute swelling; the
fibrous, nodular form is relatively benign and only rarely
produces an occlusion. The secondary arthermatous calcificat-
ion occupies a space between the two a~o~e mentioned forms.
In cases with advanced calcification the walls become stiff
but the lumen of the involved blood vessel is ra.ther dilated,
.~ because calcification is preceded by luss of fluid and shring-
age of the detritus material in the arthroma. On this basis
the theory was advanced by Loffler, of foam thrombosis. With
a rapid fall in blood pressure, and the insufficient regulat-
ory capacity of the coronary arteries lost there results a
liberation of gas from the a1'6erial blood. The gas and blood
( 26)
obstructs the smaller arteries and capillaries • But one
must take into consideration that this relative dilation is
compensated for, by organization of the artheroma and cicatr-
ical sclerosis producing a stenosiS. The relative harmlessness
of calcification of the intima, but not of the media is ex-
emplified by the senile-ectatic arterial system. The degree
of involvment of the media determines the malignancy of the
artheroma. Regressive changes in the intiona with artheroma
may lead to a speCial stenosis produced by hemorrhage and for-
mation of small thrombi; ultimately they may cause an occlus-
ion. This condition however is rare. The fibrous occlUSion
plays relatively important role in chronic ooronary occlUSion,
the process is preceded by an atherosclerotic lesion of the
blood vessel. Not the soft artheromas but calcifying art-
heromas or such which under-go organization are responsible
for a fibrous occlUSion, but this condition was found less
frequently than young connective tissue. A slow obliterat-
ion of the capillaries seems to be rather the cause than the
result of fibrous transformation. Such fibrous occlusions do
not seem to have any relation to an organized th1Dombosis.
In senial sections it can be seen that the thrombosis takes
 origin from an atheromatous ulcer, the contents of the arth -
eroma being in direct contact with the thrombosis.
The possibility of an exclusive syphilitic lesion of
the coronary arteries must be admitted but is of no pract-
ical importance. Usually the syphilitic process is located
in the wall of the ascending aorta; proliferation of the in-
tLlla and cicatrization ppoduce a stenosis and resulting occ-
lusion of the ostia of the coronary arteries. It was found
in mostly young and middle aged persons. It Was found that
in young people proliferation of the intima dominates the pic-
ture, while in older people the aneurism is more frequent.
For the study of circulation as a result of coronary

..
~
occlusion, Koch and Kong, used hearts which were made trans-
parent with wintergreen oil and benzyl benzoate, the arteries
were injected with chromium. yellow gelatin. It was found
that th~ lumen of both arteries and the area supplied by
them varied considerably. Knowledge of the main anastomoses
and Variations of the course of the arteries, is essential
for evaluation of the importance of stenosis and occlusion,
in regard to the function of the myocardium. It was found
that the arterial descending artery is the one chiefly affect-
ed by occlusion of artherosclerotic origin, next most common
is the right coronary and circumflexed artery, either in the
first portion or more distally in the vicinity of the left
border of the heart. The right artery is most frequently in
V:le vicinity of the formation of the posterior descending
artery.
In cases with occlusion of the descending artery, the
deep, subendocardial 191.yers of the anterior wall of the left
( 23)
ventricle and the anterior ventricular septum are affected,
while the.circumflexed artery has relations to the deep, low-
er and lateral layers of the left ventricle. The more extern-
al and upper layers of the left ventricle on the posterior
wall, including the upper ventricular septum, are supplied
chiefly by the right coronary artery; hence the right ventri-
cle except its part in the ventricular septum is relatively
rarely affected. Occlusions in the right coronary are
found chiefly in its peripheral portion in which the branches
sUP9ly not the right but the left ventricle. This gives the
pathological changes in coronary disease, even here Koch and
Kong admit that pathology is not found in all cases of an-
e12)
gina pectoris and is probably the result of a spasm. Now
let us consider the second part of the vascular system, that
is the incipient portion of the aorta. We can consider path-
ological changes heEe as of three sources of origin, first
athermatous changes, second syphilitic aortitis, and third
the non-speclfic inflamatory diseases associated with nec-
( 35)
rosis of the media. The clinical picture of these dis-
eases is sufficiently kno'Nn, but their consequences in the
pa.tho-phy siologic sense remain to be speci fied, especially as
regards syphilitic aortitis in its incipient stage, arther-
oscJ.-erotic changes are present almost regularly in old people,
causing but little trouble and non specific aortitis is rath-
( 18)
er rare.
In discussing the patho-physio1ogica1 changes of the
aorta the first noticab1e change is an accentuated second ao-
rtlc sound. The cause for this is an increased tension of
the vascular wall, which in turn, depends, in the presence
of a normal blood pressure, upon an increase of the vascular
caliber, decrease in thickness of the wall, and an increase
in the electricity modulus. An increase in the electricity
modulus is observed in syphilitic aortatis before any morph-
Ological change can be found, while in sevenely atheroscler-
otic or non-specifically changed aortae may still possess
their normal extenSibility. With an increase in the electri-
city modulus in the presence of a normal blood pressure im-
pairs the air chamber function of the aorta. This increases
the insufficiency volume and so decreases the coronary cir-
cUlation. To prove this Hochrein constructed a model having
the same circulatory possibilities as the Sinus Valsalvae
and the incipient portion of the aorta and to which an air
chamber wap attached. In a site corresponding to the coron-
ary orifices, an outer tube permitted measuring of the inflow
pressure or of the fluid allowed to flow in. The peripdical
perfusion WaS regulated by a "r hythmizEltion" constructed by
Braemser. The pulse rate, speed of the stream from the heart
to the aorta and the size of the air chamber function, the
aortitic and coronary pressure and circulation could be var-
 ied. By increasing the volu;Je 50-100% passing through the
aorta, while at short intervals had little effect, but accum-
ulating with time may lead to cardiac insufficiency, as
shown in table below.
PUlse Beat Maximal aortic PhlsioloSic insufficiencl vol~
rate volume cm. of water Pressure with Without air
c c air chamber chamber
68 40 50 0.70 1.00
68 40 70 0.70 1.08
68 40 90 1.00 1.15
68 80 50 0.49 0.58
6e 80 90 0.60 0.65

A further injurious moment the fact, shown in the table below,

that the blood supply of the coronary arteries in the absence
of the air chamber is effected under higher pressure and in
unarranged jets, while it is continuous and smooth in the
presence of an air chamber. It is obvious that under such con-
di tions, ·the heart cannot adapt itself to a greater strain,
since the indispensable premise for it, aamely, an increased
coronary circulation 1s not given. Greater strain and impos-
sibility for the heart to adapt itself are therefore the ca-
( 18)
uses cardiac insufficiency resulting form aortic involvement.
Pulse rate per '11inute. ..._ _
With air chamber Without air chamber
Aortic pressure Coronary Coron- Aortic Coronary Coronary cir=
in cm.of' water pressure ary press- pressure cu1ation in co
, in cm of cir- ure in in cm of per minute
water cc per em of water
minute water
S3.5/47.0 52:574'b.O C90 53 •f51.=33=-.-=5"--::::j""'-4' • 3/ 34 • 0 720
72.°/66.5 69.5/63.0 1000 72.0/51.5 73. /51.0 6 8dO
95.0/90.0 92.0/86.0 1150 92.0/70.5 94.5/71.5 1030
110.0/105.0 107 .0/103.0 1120 110.U/88.0 112.0/880 1060
liochrein concludes that the theory of aortalgia cannot be gen-
eralized, as has been shown by a large autoptically controlled
material; the coronary theory is limited by the fact that an-
gina pectoris does not at all appear each time the anatomic
conditions are given. But he does show how the condition is
(18)
brought about that is loss of the elasticity of the aorta.
Biger and Parode found that contraction of the heart had
no decreasing effect on coronary flow, but on the contrary an
increase, beginning at systole and an maximum flow was found
at the height of systole. And so against Hochreints idea that
excessive activity of the heart lead to insufficiency, they
( 30)
found that cardiac contraction promoted the coronary flow.
Now the last factor to be considered from local patho10g-
iea1 changes is the cartimac musculature. Buchner made studies
of ten patients who had attacks of angina shortly before death.
Necrotic foci were found in all cases, although the macroscop-
ic inspection did not reveal any pathology. Attacks Which oc-
curred a considerable time before deabh left traces in the form
of cicatrices. The necrotic areas were found chiefly in the
inter"na1 layers of the left ventricle, particularly in its
papillary muscles and trabeculae. Myocardial necroses of re-
cent origin were located mostly in the vicinity of older foci.
Large defects at the myocardium may o;riginate from a conflu-
ence of a few foci of various a9:es. The cause of predilect-
ion of the above mentioned areas for necrosis may be due to in-
volvement of the corresponding areas of the coronary system,
however, this theory can be applied onl.y to cases of coronary
sclerosis, but not to patien~s with syphilitic stenosis of
the coroneTY ostia; peculiarities of the distribution of blood
vessels or variations of functional demands by certain portions
of the myocardium may be responsible for the frequent lesions
(8)
of the internal layers of the left ventricle. An anemic
infarct of the myocardmum may also be produced not only by an
embolic or thrombotic occulusion, but also by a prolonged sp-
aem of one coronary artery which may lead to anemia and make
possible necrosis of a circumscribed region, which may later
become complicated by inf'lammatory changes. In the cases where
the foci of softening are situated close to the surface there
develops simultaneously a fibrinous inflamation of the perica-
rdium an epistenocardiac epicarditis. If the patient does
not die during an anginous attack there occurs a substitution
of the f.~ouS.6f:softening by connective tissue, the myocard-
ial wall becomes thinner and in some cases a cardiac aneurysm
( 13)
develops.
But Buchner does not agree to the spasm as a cause of the
necrosis, he says that under these conditions, a strain is
thrown on the heart and indirectly on the coronary circulation
influenced by the vagus nerve, and so anatomic changes take
(8)
place with a resulting ischemia not of a hypothetic spasm.
He states that the pain is result of the cardiac muscle squ-
eezing out the products of autolysis from infarcted areas
with a resulting irritation of the sensory terminal app~-
 atuses in the heart.
Now that we have discussed the local pathology and physio-
pathology, we can now turn to the final analysis, namely the
autopsy records.
Verdon collected -autopsy reco:,ds 01' cases of anging pec-
toriS, from Tocchi, Sir John Forbes, Botain, Gothwair, Buchard,
and Olsen. This group included 283 cases. They found corona
ary diseases in 50.1%, while no coronary ch8.nges were found
in 49.9%. But this WaS undoubtedly a macroscopic study and
limited to a study of only the coronary arteries, not mention-
( 36)
ing the cardiac muscle.
Then Dr. Harlow Brooks collected autopsy records, with-
out regard to angina pectoriS or heart disease. The 8,vera~e

age being 45 years. In 398 cases with all kinds of causes of

death, he found corona;ry disease in 270, 0.11 73.3%. So he con-
eludes that angina pectoriS is not dependent on coronary path-
ology since such a high percent present coronary disease,
(37)
without all having ang;ina. Desportes examined many bodies
over 50 years of age and found COr0118.I'Y athrema '; t least as
common in women as in men. Thoree says "Life is otten pro-
longed '8'i th both coronaries closed, and yet without anginal
pains. t1 But he gives no specific incidence. But Dr. Samuel
west reports a case in which one coronary is stopped and the
ot,her or:i:'ice so minute no blood could hcwe traversed it, to
get to the heart, yet there were not anginal pains. Sir C1i-
,~- fford concludes tlThat disease of the coronary arteries does
 .$/

not set up angina, is an axion founded on universal exper-

( 36)
lences. 1I
So we are forced to turn away from disease of the heart,
aorta and coronary arteries as the etiology of angina pectoriS
and look for other reasons.
Physiology has shown that there must be a proper balance
between energy taken in and energy expended. The heart muscle
receives its nurishment by means of the coronary arteries mahn-
1y as stated earlier in this paper, but a great amount comes
through the endocardium by the Thebesian vessels. The reason
that makes one sure that angina pectoriS is associated with
the heart, although the attack lacks all the physical signs,
as pulse change heart rate and regularity, and B.B. changes,
only pain, and anxiety being present, is the electrocardiogr-
aphic changes the same as found in coronary thrombosis. H.L.
Otto did experimental work on dogs. He put a ligature around
the right coron",ry artery and inverSion of "Til wave and fus-
ion of "S.T. tJ waves resulted. On ligating the left coronary
( 22)
artery he found an incrElase of the "TI! wave.
Dietrich was able to show by animal experiments, that the
characteristic electrocardiograph changes o:.;cur when a mis-
proportion is created between the volume of the blood paSSing
the heart and activity of this organ, it is ltmmaterial whether
the misproportion is due to limitation of the blood flow with
normal activity of the heart or to an increased cardiac funct-
i~n TI:th a failure of adjustment of circulation. The charact-
eristic changes c~nsist of a negative final fluctuation and
the S T interval; they serve as an expressi~n of an insuffi-
( 5)
ciency sup'Jly of 0 2 • This was proved by subjecting anim-
als to air poor in oxygen.
Buechner, ~ranz and von Lucadow and Walter performed ex-
periments 011 rabbits. These rabbits were forced to run in an
electrically driven cylinder after having been subjected to an
acute anemia which injuried the entire circu&ation including
the coronary circulation. It was pOinted out by various in-
vestigators that the electrocardiographic characteristic of the
maj or coronary infarct, namely, a neg~3_ti ve ST and T, e special-
ly in the first and second leads, were seen to appear tempor-
ar~lY in short attacks of angina pectoris. With the study of
the rabbit under the same conditions. Duchosal and Luthis el-
ectrocardiograph, whiCh writes in ink, with an electromagnetic
oscillograph was used at first, later one with an electro-
dynamic oscillograph for the purpose of longer excursions.
The results were as follows. The mere withdtrawalof 1/5 if tge
total blood caused a negative ST and T waves to appear in .the
electrocardiagram for about one hour. When the anemic animals
were forced to run the typical changes appeared regularly in
the first lead, immediately after the strain, and sometimes in
the second lead. The changes returned to normal within 24 1:10-

urs. Next nJrmal animals Viere taken and forced to run until
they were eXhausted, and the regular ST and T waves appeared
but ~nly remained from 3 to 10 hours. On examining the hearts
 ( 11)
multiple necrosis or young cicatrical areas were found.
In attacks of angina pectoris in the h~man similar chang-
es occur as reported by Feil and Siegee. Th~y tell of 2 cases
while d.uring an anginal attack there were inversion of the ST
( 21)
waves and a return to normal ~o'llbwing
. .",.--
the attack. Of a
104 patients study by Eppinger and Levine only 20 cases showed
a normal curve during an attack, the others being characteris-
( 14)
tic.
So from the above discussion we may assume that the cause
of angina is a disproportion between the volume of blood pass-
ing through the heart and the activity of the organ. The fore-
most explaination today is that of anoxemia, due to a circul-
atory deficiency. The fact the 02 properly administered re-
lieves the pain in coronary thrombosis gives a baSis. Roth-
child and Kissin assume ths.t pain in angina pectoris arises
from a localized sensi ti 'Ie area 'tihich is affected by a numeer
of stimuli. They noticed that in some cases pain appears only
at t~e beginning of effort, and if the same patient starts
slowly, he develops no pain. So they assurae that the patient
is unable to "Shift Gears" quickly enough. That there is too
sudden a nutritional demand by the myocardium and so initates
the pain. They also noted that cold acting as a peripherial
vasoconstrictor, often caused many anginal patients to develop
pain. And so it is With many patients who develop a coronary
thrombosis during an anginal attack, are relieved of their ang-
r~ i:aal pa.1n following it. This they say is the res,ult of the
 sensitive area being replaced by fiberous tissue. With these
observations and explanations they set out to confirm them.
They started out to investigate the efrect of gradually induc-
ed anoxemia. For this two groups of persons were chosen. They
chose 46 cases, the first were controlled cases, that is first
normal individuals with no history of precardial pain and no
symptoms referrable to the heart. Second individuals without
precardial pain, but subjective complaints related to the cir-
cUlatory system, with objective evidence of cardiac disease,
and third mndivil.daals ha,,1Lngca> Eli story of pain in the left
chest not due to impair.ed coronary circulation, but diagnosed
spondylitiS, brachial neuritis, rheumatic conditions etc. The
second group was the individuals with true anginal attacks.
This group they divided as follows. First individuSl,ls with
a history of precardial pain and with objective evidence of
myocardial disease aS,enlarged heart, hypertenSion, harsh
systolic murmurs and dilation or sclerosis 01' the aorta. Sec-
ond individuals with a history of precardial pain, but with
( 23)
slight or no evidence of myocardial disease. They then
constructed an apparatus which by means of soda lime theycon-
trolled the CO 8,nd also by rebreathing the air. The patients
2
were told nothing about what to expect and ask only leacUng
questions after the test. The results were as follows; None
of the control group developed pain. Of the 26 patients suff-
ering from angina pectoris, 18 developed precardial p8.in during
,,-. induced general anoxemia, and 8 did not. But the experiment
 Was not continued beyond the point of evident discomfort, so
they think the 8 would have de~eloped symptoms if the experi-
ment hed continued. It was found that pain did not appear un
til the oxygen level was down to 7%, one went to 5.9% before
( 23)
pain appeared, while the 8 did not get down below 8% of oxygen.
Dietrich and Schwiegk assume anoxia as cause of angina pector-
is and this was brought out by exposing anginal patients to
( 2:5)
a negative pressure o~ air poor in oxygen. With the fore
going experiments it seems rather evident that angina pectoris
is caused by anoxemia of the cardiac muscle. Just how this
coadition is brought about, is the next comstldl.eration. That
pain in 8.ngina pectoris is produced by the same modus operandi
as in coronary thrombosis has been shown in this paper'; to be
generally accepted. Parkinson states that "the claim ti+at
the coronary arteries are the source of anginal pain seems to-
day \lI/'ell nigh uncontested.'~o)The question is whether it is ca-
used by a spasm of the artery or by partial occlusion.
Spasms are in the bbdy, as have been seen in ocular vess-
als, with the ophthalmoscope. The result of spasm is evident
in Raynard's disease, and as it can be felt in intermittant
claudication as shown by a case reported by Lauda. l:l.e had one
patient that had intermittent claudication in his left leg
1'7hl:ch gradually increased in intens i ty for two years until on
admittance to the hospital, he ~egan to complain of precardlal
distress. On the third day after admittance he had A'>vo-l1ent
~, s tarnal pain, and two days later he died. (9) Thi s seems
to show the spastic tendency of the vascular system.
Gulengri tz and Jaraslow attempted to show by experiments
that the pain is a result of a coronary spasm. They used dogs,
and used the blQ'od pressure as an indication of pain. Sensa-
tions of pain originating in the heart are carried to the cen-
tral nervous s~stem by way of either the pressor or depressor
nerves; a modere,te stimulation is carried through the pressor
system while intense stimulation travels through the depressor
system producing a diminuation of the peripheral blood pressure.
In previous experiment s they found that sensation of pain in
the liver and kidneys is caused not by contraction, but by di-
lation of the corresponding ducts. This being a theory as ad-
vanced by Wenckebrach and upheld by Kutschera. They believe
that pai~l originates by the dilation of the aorta or the
first portion of the coronary arteries. While they do not say
t~_at spasm is not present, they claim that the spasm causes a
stasis and this in turn dilates the portion of the artery
proximal to the spasm and so pain results. So they claim that
an increase in pressure CB..n produce the necessary dllation to
( 2) .
cause 9ain. But this opinion is held only by a feiv. Guber-
gritz and Jarsolow followed the opinion of most authors in that
l'Ai'"
the heart,is locB.ted along the descending branch of' the corOl1-
ary artery. They then ligated this artery as from the atrio-
ventricul&,r syptum because of important nerve nodes located
(4 )
there ',','hieh mlght ineerfere . .7i th the -results of the eKaeriruents.
The peripheral blood pressure waS determined before,
during and after lip;8,tion and thus the presence or absence of
pain could be detec*ed. A dilation of blood vessels was pro-
duced in one series of experi~ents by the introcution of a thin
cannula into the ligated blood vessel above the ligature and
injection of a physiologic saline solutio.n through this can-
nula; thus a dilation of the proximal portion of the blood ves-
sels. In the second series of experiments two ligatures, five
to six centimeters fDom one another, and a cannula introduced
between them, this being done to prove stasis Vias not the cause
of ~$.in, but that the constriction from the ligature plus prox-
imal dilation was the cause. The experiments were performed on
14 dogs a cannula was introduced into one of the femoral art-
eries and connected with a Xymographion. In a number of cases
artificial respiration had to be employed, and this interfered
some with electrocardiographic records. Then saline solution
Was introduced very slowly and dila:iDI1 of the vessels was only
mo;;erate and did not produce changes in the blood pressure im-
media.tely but the rnotor effect took· place a few seconds after
injection with a fall in blood pressure. It could not have rce-
suI ted by changes in the >.nyocardium, as the time was too short
for sufficient change to take place. This latent period tend-
ing to prove participation of the nervous system. The consider-
able fall or blood pressure shows that evidently the se.nsatio:rj
of pain is transferred by the depressor system. They conclude
that the coronary arteries are the site of anginal pain, but
tha.:t-,the dilation and not the spasm was the cause of the stim-
ula ti on. & tthey agree wi th the spasm concept and explain it
that the spasm causes a dilation proximal to the constricted
area. Kutschera and Aichbe:cgen found a dilation of the proxi-
mal portion of the coronary vessels in many autopsies of indi-
viduals that die<m of angina pectoris. They further say that a
lesion of the myocardium may cause pain but not of the inten-
sity of a true angina pectoris. Involvement of the coronary
arteries will produce pain only if the artery did not lose its
( 14)
elasticity and ability to dilate. This seems to point out
that severe arthroma and sclerosis of the corontiries cannot ~:~

cause pain because they have lost their elasticity. Katz says
the pain of angina pectoris is due to a spasm of' coronary art
eries ds ischemia, the latter being attributed to a reflex
spasm of the coronary vessels dependent on an increased irrit-
abi Ii ty of nerve s and nodes in the walls of the se ves sels. 'rhe
nervous system ']lay exort an influence on the lumen of the cor-
( 3)
onary vessels directly. This view is also upheld by Bosco.
He did his -Nark on aef\ophagi4, in relation to gngina pectoriS
and he concluded that it is a feflex of the vegetative nervous
( 17)
nature. The influence on the J..umen of bhe coronary arteries
was thought to be hormonal. Shwarzman supposes that the musc-
ulature activity, produces a hormone, which enters the blood
stream and prevents S.lasm of' the coronary a~teries, but in dis-
ease of the somatic muscle this haromone is lacking and so the
( 32)
spasms occur. Bridges also advances a new metabolic theory
-t.hat increased blood uric acid is the cause of angina pectoris.
So he took patients with angina and ~ound the uric acid to be
4.7 mg. per 100c c as against 3.1 mg. per 100 cc in the normal
person. He treated nine cases with s5licylates in a watery
solution, these cases were not selected only as far as having
as angina pectoris. In these cases studied all recieved relief,
some complete in as short as 8 days, e,s the uric acid dropped
to ~ormal li~its. He thinks uric acid is not the sole factor
( 38)
but the disease is a metabolic disturbance.
Klemperer was able to show that reflex spasms of the coron-
ary arteries of pl3.ychic origin :nay produce myocardiac lesions
caused by local ischemia. (3) Gibson says,"True angina pectoris
results from reflex, vasomotor, neurashhenic,';and hy~terical
( 34)
casues is now beyond the region of a doubt. Lian speaks of
f'ul1ction8,1 angar, and he divides it into reflex angan which may-
be considered as a result of aerogastria, cholethiases thor-
acobrachial neuralgia, then his neurotic angar and toxic angar
(16 )
due abuse of nicotine 'etc. Schmidt theDry is that angina
pectoris is result nerve envolvement, and camms it the vaso-
motor-neur~genous theory. His argument is the presence of fi-
rst painful potnts in angina pectoris, located in tbe areas of
the 1st to 5th dorsal vertebrae and left brachial plexus is
sensi ti ve to touch. Se cond he finds a certain analogy between
angina 98ctoris and other neurologic conditions as neuralgia
( 1)
of the trigeminus nerve or sciatica. 1'rei th~r of the se obser-
vations seem to be upheld by other men except Rudnitskiy, who
s~ the vasomotor com:Jonent of Schmidt's theory cannot be dBn-
 ied.
In assuming that coronB.ry spasms are the cause of angina
recent surgical treatment has been employed, on this basis.
It is based on an interruption of the paths along which in the
anginous attack, the stimulations originating from the heart
and give rise to pain and anxiety. It has been found that the
most important paths course in the cardiac rami over the stell-
ate ganglion to the spinal cord. At the ganglion a separation
of rami communicantes from eight cervical to 4th dorsal,blocks
effiCiently and without difficulty the transmission of impulses.
The stellate ganglion and the imoortant motor fibers passing
- (4)
from it t~ the heart are left intact. But this has merely the
Same effect as a card.tomy for the relief of pal~but it is
doubtful if it cures the site of trouble in the heart. With
the cause of angina pectoris as a result of anoxemia, which is
quite definitely proven, attention has been turned these last
few years to thyroidecto'TIY for heart disease. This proceedure
was started in 1932 in Boston by Blumgart and his coworkers.
The principle is based on the fact that the rate of metabolism
is ~overned by the thyroid gland, although ';:his is still ques-
tionable. So if the thyr')id were removed, the metabolic rate
is lowered; with the lowering of the metaholic rate there is
a diminished demand ~or oxygen by the tissues; if the oxygen
requirements are lessened the demands on the circulation are
diminished. While a damaged heart caTh."1ot carry the full cir-
,~ culatory load 0: normal mettabolism, it maybe able to carry
 "II

( 4)
the 6Qmplet.-~ load)ot a.~lawered metabolism. Cutler and
Schni tker report 29 Cctses ',vhich had a total thyroidectomy for
angina pectoris since Dec. 1932. Of this series 21 patients
in whom the postoperative period of observation was from two
and one-fourth months to 16 months, showed improvement. The
amount of relief was gauged as follows; 47.6% improved from
90-100%; 66.6'10 improved from 75-100%; 90.4% improved over 50%
( 42)
and only 9.5% improved less than 50%.
Mixter, Blumgart, Herman and Berlin report 75 cases of
angina pectoris treated by total thyroidectomy showing quite
( 41)
similar results. It has been found by these men, that all
thyroid tissue must be removed if permanent hypothyroidism is
to be prt.:;sent and a lowered metabolic rate result. So in
attempting to draw 8,ny defini te conclusi::m it is going to be
quite difficult. A few things seem certain. Pathological
changes in the aorta and coronary areeries is not the cause
of al1~ina pectoris as autopsy records show, but m.ay be a com-
plicating factor~ With the brilliant work recently done on
anoxemia it seems to me to leave li ttle quest,ion that thi s is
the, cause of anginal pain. As to how this conditi'Jn is br-
ought about there still seems to be a question. It seems sin-
ce pathologlcal changes do not cause angina pectoris, then it
must be a functional condi tim. The only avenues left would
be metabolic, hormonal, nervous, or coronary spasm. :let lit-
:tie evidence has been advanced to uphold the hormona.l and me't-
,..-. abolic theories. So this leave s only the coronary arteries and
their nerve control. I believe that the general trend of
moat authorities is leaning toward the theory of coronary
spasm as I have previously quoted, as the fundamental cause
of angina oectoris, whether this condition be of local origin
or from nerve control has not been worked out as yet.
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